Pandemic of Obesity and MetS
The prevalence of obesity and associated metabolic disorders such as hyperlipidaemia, hypertension and impaired blood glucose regulation, commonly referred to as the metabolic syndrome (MetS) has reached pandemic proportions and is a major contributor to the burden of disease world-wide. Approximately 1.6 billion adults are over-weight or obese. Currently about 366 million people are diagnosed with type 2 diabetes, and the prognosis for 2030 is 550 million. If including also other disturbances in the MetS, it is presumed that more than 30 million people in Europe and about 85 million in US receive medication for various manifestations in this syndrome. The cause for the obesity and diabetes pandemic is not fully known, but dietary factors play a major role. A common feature associated with obesity and MetS is a state of low-grade inflammation, and concomitant resistance to insulin.
Alike the situation in adults, obesity among children is an increasing problem in many countries. It is known that presence of obesity in early age is associated with increased risk of obesity in adulthood. Also, metabolic disturbances already at a low age appear to be particularly detrimental. Thus, obesity in childhood seems to cause type 2 diabetes within a shorter time period compared to the situation in adulthood. This vulnerability of obese children possibly runs in parallel to the over-all anabolic situation associated with growth in the child. According to a recent global estimate, about 170 million children are over-weight or obese. The prevalence of obesity and over-weight among pre-school children in Sweden is about 18%. Of interest in this respect is current knowledge indicating that approximately half of the European children with obesity or over-weight show elevated cardio-metabolic risk factors already at onset of puberty. According to studies in US, about 15% of obese children even display advanced MetS features such as non-alcoholic fatty liver disease.
Several large scale observational studies have demonstrated that healthy young subjects with more body fat or higher BMI have moderately higher concentrations of inflammatory markers than leaner control subjects. This is in support of the view that obesity should be considered as a state of chronic low-grade inflammation also in the young. In fact, accelerated formation of reactive oxygen species and accumulation of oxidized macro-molecules have been demonstrated in juvenile overweight and obesity.
Dietary Factors Influencing Risk Factors and Disease Development
Dietary factors are considered the single most important for development of obesity and MetS. A key factor involved in the ethiology of the MetS, is low grade inflammation. This inflammation is triggered by over-eating, but also by very specific features related to the quality of foods and meals. One example of such features includes the potency of the carbohydrates in foods to increase postprandial blood glucose after a meal. The effect of different carbohydrate foods on blood glucose response is commonly ranked by use of the Glycaemic Index (GI). The GI is defined as the incremental area under the blood glucose response up to 120 min after the test product as a percentage of the same area following ingestion of a carbohydrate equivalent amount of a reference (glucose or white bread) by the same subject. Another quality aspect of importance in relation to the inflammatory properties of food relates to its content of compounds formed during heat-processing and storage of foods containing protein and carbohydrates, so called Maillard reaction products.
From studies in healthy adults we know that not only may the amount of protein be important for the insulin response, but also the quality of the proteins. One aspect on protein quality is the process-induced loss of certain essential amino acids (e.g. Lysine), due to the Maillard reaction between proteins and reducing sugars. Later stage products of the Maillard reaction are collectively called advanced glycation end products (AGE), and they have been put forward as promotors of oxidative stress and low-grade inflammation.
In a recent report it was concluded that carbohydrate quality and quantity may influence blood lipid concentrations and inflammation in non-diabetic subjects. Consequently, high GI diets cause postprandial hyperglycaemia which in itself is an important driver of oxidative stress and inflammation. Of interest in this respect is that differences in GI of meals may influence acute formation of inflammatory metabolites, not only in diabetes, but also in young healthy subjects. Available knowledge indicates that GI of foods is ranked similarly in adults and in small children, emphasising the global importance of the GI concept across age.
During excessive heat processing of a carbohydrate source, it may be transformed into a more rapidly digestible form, causing high postprandial glycaemic responses. The potential reason for a quality loss of the carbohydrates during such conditions is that important structural features of the raw material is partly degraded, and the starch completely gelatinised and partially solubilised. Another hypothesis about how hyperglycaemia causes inflammation and vascular damage is that the high blood glucose levels promote endogenous formation of AGE products, which are described above.
As evident from the high and rising prevalence of obesity and MetS, preventive measures are needed. This calls for strategies focusing on the quality characteristics of the diet directed in particular towards the young, where infants and small children constitute a particularly important target group.